Effect of 17 β-estradiol on calcium response to phytohaemagglutinin in human lymphocytes

1990 ◽  
Vol 10 (1) ◽  
pp. 73-78 ◽  
Author(s):  
Tiziana Bellini ◽  
Diana Degani ◽  
Maurizio Matteuzzi ◽  
Franco Dallocchio
Keyword(s):  
Cell Surface ◽  
Steroid Hormones ◽  
Human Lymphocytes ◽  
Cytosolic Calcium ◽  
Free Calcium ◽  
Cytosolic Free Calcium ◽  
Calcium Response ◽  
Pre Treatment ◽  
Preincubation Time ◽  
Estradiol Concentration

Pre-treatment of human lymphocytes with 17 β-estradiol diminishes the increase in concentration of cytosolic free calcium after stimulation with phytohaemagglutinin. The effect is dependent on 17 β-estradiol concentration and on the preincubation time. The effect is not due to an interaction between 17 β-estradiol and phytohaemagglutinin, but appears to be a consequence of the binding of the hormone to the cell surface. The effect is specific for 17 β-estradiol, since the α isomer and other steroid hormones (progesterone, testosterone, diethylstilbestrol and 5α-androstan), have no effect. Since the effect of the 17 β-estradiol can be suppressed by treatment of lymphocytes with ouabain, it appears that the effect of estradiol on the rise of cytosolic calcium induced by phytohaemagglutinin is mediated by the (Na, K)-ATPase.

Myelin Basic Protein inhibits the calcium response to phytohaemagglutinin in human lymphocytes

1990 ◽  
Vol 10 (1) ◽  
pp. 55-59
Author(s):  
Tiziana Bellini ◽  
Diana Degani ◽  
Maurizio Matteuzzi ◽  
Franco Dallocchio
Keyword(s):  
Myelin Basic Protein ◽  
Protein Concentration ◽  
Basic Protein ◽  
Human Lymphocytes ◽  
Cytosolic Calcium ◽  
Free Calcium ◽  
Cellular Activation ◽  
The Central Nervous System ◽  
Pre Treatment ◽  
Preincubation Time

Myelin Basic Protein, one of the major membrane protein component of the central nervous system, was used to probe the molecular mechanism of cellular activation by phytohaemagglutinin. Pre-treatment of human lymphocytes with myelin basic protein results in a lower rising of cytosolic concentration of free calcium after stimulation with phytohaemagglutinin. This effect is dependent on myelin basic protein concentration and on the preincubation time of the protein with the cells. It is not due to a interaction between myelin basic protein and phytohaemagglutinin, but appears to be a consequence of the binding of the protein to the cell surface. The reduction of the rise of cytosolic calcium induced by phytohaemagglutinin is specific for the myelin basic protein because other proteins like albumin and protamine have no effect.

Angiotensin II causes sustained elevations in cytosolic calcium in glomerulosa cells

1988 ◽  
Vol 255 (3) ◽  
pp. E338-E346 ◽  
Author(s):  
R. E. Kramer
Keyword(s):  
Angiotensin Ii ◽  
Calcium Concentration ◽  
Cytosolic Calcium ◽  
Calcium Signal ◽  
Free Calcium ◽  
Cytosolic Free Calcium ◽  
Cytosolic Calcium Concentration ◽  
Free Calcium Concentration ◽  
Cytosolic Free Calcium Concentration ◽  
Glomerulosa Cells

Studies were conducted to examine the effects of angiotensin II on cytosolic free calcium concentration in bovine adrenal glomerulosa cells maintained in primary culture. The calcium indicator, fura-2, and discontinuous dual-wavelength fluorescence spectroscopy were used to measure cytosolic free calcium in superfused adherent cell monolayers. Basal cytosolic free calcium concentration was 63.7 +/- 3.3 nM. The threshold concentration for angiotensin II-stimulated increases in cytosolic calcium was 10(-14)-10(-13) M, and maximal elevation of cytosolic calcium was produced by 10(-9) M angiotensin II. Angiotensin II (10(-13) M) produced a gradual increase in cytosolic calcium concentration that plateaued after 3-5 min of superfusion at a level approximately 1.2 times that of control cells. The calcium signal invoked by a maximal concentration (10(-9) M) of angiotensin II, in contrast, was characterized by an immediate, intense (approximately 8-fold) increase in cytosolic calcium concentration that decayed within 5 min to a lower, but sustained, level 2.5-3 times that of control cells. The calcium signals invoked by intermediate concentrations (10(-12)-10(-10) M) of angiotensin II exhibited dose-dependent increases in magnitude and a gradual transition in nature between those invoked by threshold and maximal concentrations of the peptide. The effect of angiotensin II to increase cytosolic calcium concentration was accompanied by an increase in aldosterone output. The increase in steroidogenesis was most closely correlated with the magnitude of the initial calcium signal. At high concentrations (10(-10) and 10(-9) M) of angiotensin II, there was a clear dissociation between aldosterone output and the magnitude of the sustained calcium signal.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Flow cytometric analysis of murine splenic B lymphocyte cytosolic free calcium response to anti-IgM and anti-IgD

Cytometry ◽  
1987 ◽  
Vol 8 (4) ◽  
pp. 396-404 ◽  
Author(s):  
Thomas M. Chused ◽  
H. Alexander Wilson ◽  
David Greenblatt ◽  
Yasuo Ishida ◽  
Linette J. Edison ◽  
...  
Keyword(s):  
B Lymphocyte ◽  
Flow Cytometric Analysis ◽  
Free Calcium ◽  
Cytosolic Free Calcium ◽  
Calcium Response ◽  
Flow Cytometric

scholarly journals Hypertension Secondary to PHPT: Cause or Coincidence?

2011 ◽  
Vol 2011 ◽  
pp. 1-6 ◽  
Author(s):  
Helmut Schiffl ◽  
Susanne M. Lang
Keyword(s):  
Cardiovascular Reactivity ◽  
Vascular Reactivity ◽  
Cytosolic Calcium ◽  
Free Calcium ◽  
Normal Blood Pressure ◽  
Cytosolic Free Calcium ◽  
Hypertensive Patients ◽  
Before And After ◽  
Underlying Mechanisms ◽  
Normal Controls

Primary hyperparathyroidism (PHPT) may be associated with arterial hypertension. The underlying mechanisms are not fully understood and reversibility by parathyroid surgery is controversial. This study aimed to characterize pressor hormones, vascular reactivity to norepinephrine, and cytosolic-free calcium in platelets in 15 hypertensive patients with hypercalcaemic PHPT before and after successful parathyroidectomy and to compare them with 5 pre-hypertensive patients with normocalcaemic PHPT, 8 normotensive patients with hypercalcaemic PHPT and 15 normal controls. Hypertensive patients with hypercalcaemic PHPT had slightly higher levels of pressor hormones (), enhanced cardiovascular reactivity to norepinephrine () and increased cytosolic calcium in platelets () than controls. Pre-hypertensive patients with normocalcaemic PHPT had intermediate values of increased cardiovascular reactivity and cytosolic calcium. Normotensive patients with hypercalcaemic PHPT and normotensive controls had comparable pressor hormone concentrations and intracellular calcium levels. Successful parathyroidectomy was associated with normal blood pressure values and normalisation of pressor hormone concentrations, cardiovascular pressor reactivity and cytosolic free calcium. Our results suggest that parathyroid hypertension is mediated/maintained, at least in part, by functional alterations of vascular smooth muscle cells and can be cured by parathyroidectomy in those patients who do not have primary hypertension.

scholarly journals Calcium Regulates the Association between Mitochondria and a Smooth Subdomain of the Endoplasmic Reticulum

2000 ◽  
Vol 150 (6) ◽  
pp. 1489-1498 ◽  
Author(s):  
Hui-Jun Wang ◽  
Ginette Guay ◽  
Liviu Pogan ◽  
Remy Sauvé ◽  
Ivan R. Nabi
Keyword(s):  
Confocal Microscopy ◽  
Mdck Cells ◽  
Close Association ◽  
Cytosolic Calcium ◽  
Free Calcium ◽  
Autocrine Motility Factor ◽  
Cytosolic Free Calcium ◽  
Motility Factor ◽  
Rat Liver Cytosol ◽  
Close Contacts

Association between the ER and mitochondria has long been observed, and the formation of close contacts between ER and mitochondria is necessary for the ER-mediated sequestration of cytosolic calcium by mitochondria. Autocrine motility factor receptor (AMF-R) is a marker for a smooth subdomain of the ER, shown here by confocal microscopy to be distinct from, yet closely associated with the calnexin- or calreticulin-labeled ER. By EM, smooth ER AMF-R tubules exhibit direct interactions with mitochondria, identifying them as a mitochondria-associated smooth ER subdomain. In digitonin-permeabilized MDCK cells, the addition of rat liver cytosol stimulates the dissociation of smooth ER and mitochondria under conditions of low calcium. Using BAPTA chelators of various affinities and CaEGTA buffers of defined free Ca2+ concentrations and quantitative confocal microscopy, we show that free calcium concentrations <100 nM favor dissociation, whereas those >1 μM favor close association between these two organelles. Therefore, we describe a cellular mechanism that facilitates the close association of this smooth ER subdomain and mitochondria when cytosolic free calcium rises above physiological levels.

Estradiol binding to cell surface raises cytosolic free calcium in T cells

FEBS Letters ◽  
1998 ◽  
Vol 422 (3) ◽  
pp. 349-353 ◽  
Author(s):  
W.Peter M Benten ◽  
Michèle Lieberherr ◽  
Günter Giese ◽  
Frank Wunderlich
Keyword(s):  
T Cells ◽  
Cell Surface ◽  
Free Calcium ◽  
Cytosolic Free Calcium

Impaired cytosolic free calcium response in splenic T-cells from mice fed with ethanol-containing diet

1993 ◽  
Vol 15 (6) ◽  
pp. 647-656 ◽  
Author(s):  
Mei-Ping Chang ◽  
Dean T. Yamaguchi ◽  
Michael Yeh ◽  
Dean C. Norman
Keyword(s):  
T Cells ◽  
Free Calcium ◽  
Cytosolic Free Calcium ◽  
Calcium Response

Prostaglandin F2 alpha releases calcium from a thapsigargin-sensitive pool in ovine large luteal cells

1994 ◽  
Vol 266 (1) ◽  
pp. E50-E56 ◽  
Author(s):  
J. A. Wegner ◽  
R. Martinez-Zaguilan ◽  
R. J. Gillies ◽  
P. B. Hoyer
Keyword(s):  
Small Cells ◽  
Free Calcium ◽  
Acetoxymethyl Ester ◽  
Cytosolic Free Calcium ◽  
Calcium Response ◽  
Luteal Cells ◽  
Prostaglandin F2 Alpha ◽  
Progesterone Secretion ◽  
Sustained Increase ◽  
Calcium Pool

Thapsigargin (TG) and A23187 were used to examine the regulation of cytosolic free calcium (Cai2+) in ovine large and small luteal cells. Thapsigargin (50 nM) induced a sustained increase of Cai2+ in fura 2-acetoxymethyl ester (AM)-loaded cells (large = 1.32 +/- 0.07-fold, small = 1.45 +/- 0.07-fold, P < 0.05). A23187 (1 microM) induced a rapid transient increase of Cai2+ (large = 1.37 +/- 0.07-fold, small = 1.46 +/- 0.10-fold, P < 0.05). In large cells, 0.5 microM prostaglandin F2 alpha (PGF2 alpha) increased Cai2+ 1.54 +/- 0.11-fold. Pretreatment with 50 nM TG abolished the PGF2 alpha-induced calcium response. Pretreatment with PGF2 alpha attenuated (P < 0.05) the TG-induced Cai2+ increase. Progesterone secretion was significantly (P < 0.05) inhibited by incubation with 50 nM TG, 1 microM A23187, and 0.5 microM PGF2 alpha in large but not small cells. These data suggest that PGF2 alpha releases calcium from a TG-sensitive intracellular calcium pool in ovine large luteal cells.

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